Continuous quantitative monitoring of cerebral oxygen metabolism in neonates by ventilator-gated analysis of NIRS recordings.

Oxidative stress during fetal development, delivery, or early postnatal life is a major cause of neuropathology, as both hypoxic and hyperoxic insults can significantly damage the developing brain. Despite the obvious need for reliable cerebral oxygenation monitoring, no technology currently exists to monitor cerebral oxygen metabolism continuously and noninvasively in infants at high risk for developing brain injury. Consequently, a rational approach to titrating oxygen supply to cerebral oxygen demand - and thus avoiding hyperoxic or hypoxic insults - is currently lacking. We present a promising method to close this crucial technology gap in the important case of neonates on conventional ventilators. By using cerebral near-infrared spectroscopy and signals from conventional ventilators, along with arterial oxygen saturation, we derive continuous (breath-by-breath) estimates of cerebral venous oxygen saturation, cerebral oxygen extraction fraction, cerebral blood flow, and cerebral metabolic rate of oxygen. The resultant estimates compare very favorably to previously reported data obtained by non-continuous and invasive means from preterm infants in neonatal critical care.

Intractable sneezing: is it always psychogenic?

Intractable sneezing is not a commonly encountered disorder. The clinical presentation of such patients may cause the physician to undertake several tests before making a diagnosis. Are the performed analytic tests a waste of the health service funds or are they really sufficient? In this case, after undergoing several tests to rule out potential causes of the prevailing symptoms, psychiatric evaluation revealed a triggering event that contributed to the diagnosis of psychogenic sneezing. This specific case demonstrates why the diagnosis of psychogenic sneezing is difficult. An overwhelming number of such patients may be linked to a psychogenic cause; nevertheless, organic lesions or causes should be carefully excluded. Addressing the psychosocial issues through psychotherapy and coincidental use of locally administered anesthesia assisted in resolving the symptoms.

Umbilical Venous Catheter Malposition Is Associated with Necrotizing Enterocolitis in Premature Infants.

OBJECTIVE: The etiology of necrotizing enterocolitis (NEC) remains elusive despite known associations with several factors, including intestinal ischemia related to the effects of umbilical arterial catheterization on the mesenteric circulation. However, the role of the mesenteric venous circulation has yet to be studied as a potential cause of NEC. We examined the association between umbilical venous catheter (UVC) position and the development of NEC in premature infants. DESIGN: A prospective cohort study was performed to examine the effect of UVC on portosystemic shunting via the ductus venosus (DV) and its potential role in NEC. RESULTS: We recruited 132 premature infants, 62 of which had a birth weight ≤1,500 g. NEC was noted in 12 (19%) patients. All infants weighing ≤1,500 g underwent an attempt at UVC insertion. The UVC status was classified as appropriate (n = 39), unsuccessful (n = 9), or malpositioned (n = 14). Among the NEC patients, 7 (58%) had a UVC malposition and 3 (25%) had an unsuccessful attempt. These rates were significantly higher than in patients without NEC (14 and 12%, respectively). Multivariable logistic regression analysis confirmed birth weight (OR 2.2, 95% CI 1.2-4.7, p = 0.001) and UVC malpositioning (OR 6.9, 95% CI 1.6-35.4, p = 0.007) as independent risk factors associated with NEC. CONCLUSIONS: Unrecognized withdrawal of a UVC into the portal vein or DV is associated with an increased incidence of NEC in infants weighing ≤1,500 g. The data support the need for additional studies to examine this effect. Confirmation of a causal relationship will raise the need to reassess UVC insertion criteria and strategies for more closely monitoring the catheter tip position.

Effects of regional brain injury on the newborn autonomic nervous system.

OBJECTIVE: Cerebral mapping of central autonomic nervous system (ANS)(1) function in mature animals and humans lateralizes sympathetic and parasympathetic influence predominantly to the right and left cerebral hemispheres, respectively. Spectral analysis of heart rate variability (HRV)(2) is an established measure of ANS function. We examined whether such lateralization is present in the term newborn. METHODS: We retrospectively reviewed records of infants >36 weeks of gestation diagnosed with hypoxic ischemic encephalopathy (HIE).(3) We included infants with neonatal EEG and regional injury on brain MRI, which was scored using a schema. We extracted ECG signals from the EEG recording, but excluded periods of electrographic seizure activity to eliminate possible seizure influence on HRV. HRV was evaluated by spectral analysis in the high frequency (HF(4); 0.3-1 Hz) and low frequency (LF(5); 0.05-0.25 Hz) ranges, and the LF/HF ratio was examined to assess sympatho-vagal balance. The relation between the injured brain regions and HRV was studied using multiple linear regression models. RESULTS: We studied 40 neonates with HIE. Injury to the right cerebral cortex (p=0.009) and right cerebellum (p=0.041) predicted a decreased LF/HF ratio. Injury to the left cerebral cortex (p=0.035) and left cerebellum (p=0.041) was associated with an increased LF/HF ratio. The association between brain injury location and the individual LF or HF spectral powers of brain injury did not reach significance. CONCLUSIONS: Our data suggest that a functional lateralization for cerebral autonomic influence is established by term gestation.

Neonatal renal physiology.

The renal system plays a tremendous role in growth and development of infants and children. The kidney itself also undergoes a maturation process as it transitions from the fetal to the extrauterine environment. Renal function continues to undergo further adaptive changes in the neonatal period. It is important for the clinician caring for neonates to be aware of the expected fluid shifts, electrolyte handling, and renal functional capacity as these "normal" changes will become quite relevant when medical or surgical pathology is present. The preterm neonates are especially vulnerable due to their functionally immature kidneys. Renal function in the preterm neonate is not only immature at birth but there is a significant delay in the renal function to achieve its full capacity. This review highlights the physiologic adaptations of the kidney and its effects on the body during the neonatal period.

Ductus venosus closure results in transient portal hypertension--is this the silent trigger for necrotizing enterocolitis?

INTRODUCTION: The etiology of necrotizing enterocolitis (NEC) remains elusive and no definite trigger has been identified. There are no studies to date examining the potential role of closure of the ductus venosus (DV), its effect on increasing portal venous pressure (PVP) and its association to mesenteric venous ischemia in the development of NEC. Our aim was to develop an animal model to examine this physiology. METHODS: Fifteen near-term lambs were used. The DV was occluded in experimental animals by a balloon tip catheter, while the sham controls underwent catheterization without DV occlusion. Vital signs and PVP were monitored for 4h, followed by intestinal biopsy. RESULTS: The experimental group (n=5) demonstrated a significant increase in PVP following DV occlusion (11.87 mm Hg [95% CI: 11.40-12.34]), compared to controls (8.95 mm Hg [95% CI: 8.34-9.56]) (F=12.16, p=0.001). Histology of the terminal ileum showed vacuolar degeneration, indicative of reversible cellular damage in the experimental group. CONCLUSIONS: We demonstrate that DV closure in the neonatal lamb leads to transient portal hypertension which is associated with cellular damage and inflammatory changes of the intestinal mucosa. Additional studies will be necessary to determine if the transient portal hypertension following DV closure leads to clinically apparent intestinal ischemia and NEC.